The interferon-alpha (IFN-alpha)-stimulated gene factor 3 (ISGF3), a transcriptional activator, contains three proteins, termed ISGF3 alpha proteins, that reside in the cell cytoplasm until they are activated in response to IFN-alpha. Treatment of cells with IFN-alpha caused these three proteins to be phosphorylated on tyrosine and to translocate to the cell nucleus where they stimulate transcription through binding to IFN-alpha-stimulated response elements in DNA. IFN-gamma, which activates transcription through a different receptor and different DNA binding sites, also caused tyrosine phosphorylation of one of these proteins. The ISGF3 alpha proteins may be substrates for one or more kinases activated by ligand binding to the cell surface and may link occupation of a specific polypeptide receptor with activation of transcription of a set of specific genes. ...
Our new finding of the dose‐dependent shift of signaling modes by a GPCR has several implications. G‐protein‐dependent signaling and G‐protein‐independent signaling are related by their different sensitivity to concentrations of the same agonist. The G‐protein‐dependent signaling of GPCRs is similar to receptor tyrosine kinase signaling through the small GTPase Ras. The G protein‐independent signaling of GPCRs can be compared to cytokine JAK-STAT signaling, in which non‐receptor tyrosine kinases are directly coupled to membrane receptors. Also, it is interesting to note that some seven‐transmembrane receptors, such as Smoothened in Hedgehog gradient signaling, mainly use their C‐terminal tails to directly interact with downstream signaling molecules without the participation of G proteins (Lum and Beachy, 2004). Both the JAK-STAT and the Smoothened pathways result in activation of latent cytoplasmic transcription factors. Src could mediate GPCR‐responsive changes in gene ...
INTRODUCTION Estrogen Receptor α (ERα) is a key regulator in normal mammary gland development and acts as a growth factor in breast cancer development. We have developed the CERM mouse model with targeted ERα overexpression and deregulation specifically to the mammary gland. By 4 months of age, the CERM mice develop ERα-initiated mammary ductal hyperplasia and ductal carcinoma in-situ which mimic human disease (Frech et al., 2005). In women, there is evidence that early full-term pregnancy decreases lifetime ERα-positive breast cancer risk. Paradoxically, there is also evidence that breast cancer risk is transiently increased within ten years of early full-term pregnancy (Schedin, 2006). One potential mechanism for the lifetime protective effect is believed to occur via differentiation (Russo et al., 2006). In addition, it is well established that STAT5a, a latent cytoplasmic transcription factor, is highly activated during pregnancy and lactation, and is involved in alveolar proliferation ...
Via interaction with their specific receptors, interferons (IFNs) activate signal transducer and activator of transcription (STAT) complexes. STAT activation initiates the classical Janus kinase-STAT (JAK-STAT) signaling pathway. In this pathway, JAKs associate with IFN receptors and, following receptor engagement with IFN, phosphorylate both STAT1 and STAT2. As a result, an IFN-stimulated gene factor 3 (ISGF3) complex forms-this contains STAT1, STAT2 and a third transcription factor called IRF9-and moves into the cell nucleus. Inside the nucleus, the ISGF3 complex binds to specific nucleotide sequences called IFN-stimulated response elements (ISREs) in the promoters of certain genes, known as IFN stimulated genes. Discover the latest research on interferon signalling here. ...
Recombinant Human STAT1 protein Full length protein datasheet (ab82610). Abcam offers quality products including antibodies, assays and other reagents.
References for Abcams Recombinant human STAT2 protein (ab81880). Please let us know if you have used this product in your publication
Today, scientists know that the JAK-STAT pathway faithfully relays the messages of at least 40 different molecular signals, including interferon, growth hormone, prolactin, erythropoeitin and most of the interleukins - and thus constitutes one of the body s primary means of communicating with its vast multitude of cells. What happens when this communication goes awry was demonstrated by Darnell, Jacqueline Bromberg, Henriksen and other colleagues in 1999. They showed that a human STAT protein, called STAT3 - which is overactive in various human tumors - can by itself turn normal cells into cancerous ones. The finding marked STAT3 as an official "oncogene" and solidified the notion that drugs designed to block the action of STATs may prove beneficial to cancer patients ...
... returns the number of occurrences of each residue in the sequence you enter. Percentage totals are also given for each residue, and for certain groups of residues, allowing you to quickly compare the results obtained for different sequences ...
A family of transcription factors containing SH2 DOMAINS that are involved in CYTOKINE-mediated SIGNAL TRANSDUCTION. STAT transcription factors are recruited to the cytoplasmic region of CELL SURFACE RECEPTORS and are activated via PHOSPHORYLATION. Once activated they dimerize and translocate into the CELL NUCLEUS where they influence GENE expression. They play a role in regulating CELL GROWTH PROCESSES and CELL DIFFERENTIATION. STAT transcription factors are inhibited by SUPPRESSOR OF CYTOKINE SIGNALING PROTEINS and PROTEIN INHIBITORS OF ACTIVATED STAT ...
Activity:. STAT5-IN-1 is a STAT5 inhibitor with an IC50 of 47 μM for STAT5β isoform. IC50 & Target: IC50: 47 μM (STAT5β)[1] In Vitro: The signal transducer and activator of transcription 5 (STAT5) is a member of the STAT family of proteins, implicated in cell growth and differentiation. STAT5-IN-1 inhibits STAT5 by binding to the SH2 domain. The functions of the SH2 domains of STAT3, STAT1, and of the tyrosine kinase Lck are inhibited to a lesser extent (IC50>500 µM). STAT5-IN-1 block STAT5/STAT5 DNA binding in K562 nuclear extracts. Substitution of the hydrogen at C6 of the chromone ring by an ethyl group does not affect activity of STAT5-IN-1 against STAT5β, but leads to complete loss of selectivity against other STAT family members[1]. Protocol:. References:. ...
Signal transducer and activator of transcription 5 (Stat5) belongs to a family of cytoplasmic transcription factors that can be activated (phosphorylated) by a cell surface receptor. Phosphorylation at Tyr694 is obligatory for Stat5 activation. Stat5 has two isoforms, Stat5 alpha and Stat5 beta. Aberrant Stat5 activation has been implicated in the pathogenesis of chronic myelogenous leukemia, prostate and breast cancer and tumor metastasis. Stat5 is localized in the cytoplasm and upon phosphorylation at Y694 is translocated to the nucleus. Ideal for Cancer, Chromatin & Nuclear Signaling and Signal Transduction research.
Abstract: : Purpose: STAT proteins are a family of transcription factors that mediate the action of several growth factors. The purpose of this study was to assess the effect of PDGF in STAT1 and STAT3 synthesis. Methods: Primary hRPE cell cultures were established from four human eyes obtained from the Michigan Eye Bank. Cells were allowed to grow to confluence and treated with PDGF and genistein. Cell viability was determined by the trypan blue exclusion method. Cell proliferation was monitored by 3H-thymidine (3H-thy) incorporation. 14C-methionine labeled-intracellular STAT1 and STAT3 synthesis was determined by immunoprecipitation using STAT1 and STAT3 antibodies and SDS-PAGE analysis. Data were analyzed by Student t test and Wilcoxon Signed Rank test. P,0.05 was considered to be significantly different. Results: PDGF increased hRPE cell number and 3H-thymidine incorporation in a dose dependent manner. PDGF also increased 14C-methionine STAT 1 and STAT 3 protein synthesis in a dose ...
One subunit of the interleukin-6 (IL-6) receptor, which activates Janus kinases upon ligand binding, is gp130. Tyrosine phosphorylation of gp130 recruits protein phosphatase 2 (SHP2) and signal transducer and activator 3 (STAT3). Ohtani et al. utilized knock-in technology to create mice deficient in only the gp130-mediated SHP2 pathway or the gp130-mediated STAT3 pathway to dissect the roles these two pathways play in IL-6 signaling. Eliminating the SHP2 response resulted in prolonged IL-6-induced STAT3 phosphorylation. STAT3 signaling was required for embryonic development, where as SHP2 signaling-deficient mice were viable and fertile. STAT3 signaling was required for induction of astrocytes by IL-6 cytokines. Reciprocal roles for STAT3 signaling and SHP2 signaling (STAT3 providing a positive signal and SHP2 providing a negative signal) were found for cytokine and immunoglobulin responses and lymphoid organ homeostasis. Thus, mice deficient in SHP2 signaling developed splenomegaly and ...
Signal transducer and activator of transcription 3 (STAT3) is an important transcription factor ubiquitously expressed in different cell types. STAT3 plays an essential role in cell survival, proliferation, and differentiation. Aberrantly hyper-activated STAT3 signaling in cancer cells and in the tumor microenvironment has been detected in a wide variety of human cancers and is considered an important factor for cancer initiation, development, and progression. However, the role of STAT3 activation in monocytes in the development of HCC has not been well understood. Immunohistochemical analysis of phosphorylated STAT3 was performed on tissue microarray from HCC patients. Using a co-culture system in vivo, HCC cell growth was determined by the MTT assay. In vivo experiments were conducted with mice given diethylinitrosamine (DEN), which induces HCC was used to investigate the role of STAT3 expression in monocytes on tumor growth. Real-time PCR was used to determine the expression of cell proliferation and
This study showed that gp130, a member of the cytokine receptor superfamily, efficiently activates the TAK1 through the YXXQ motif in gp130, and this kinase preferentially activates the downstream kinase NLK, which is responsible for STAT3 Ser-727 phosphorylation via the YXXQ motif-derived signal. Furthermore, this study revealed a novel role for STAT3 in IL-6-induced NLK activation but not in TGFβ-induced NLK activation. STAT3 functions as a scaffold for TAK1 and NLK specifically in IL-6 signaling by binding them at its carboxyl-terminal region. The following observations support the idea that this interaction is physiologically significant: (i) most TAK1-NLK interactions in the nuclear extracts of IL-6-stimulated HepG2 cells depended on the presence of STAT3 (Fig. 5B ); (ii) the IL-6-induced NLK activation was greatly decreased in HepG2-STAT3KD cells; (iii) STAT3 and TAK1 were independently activated by IL-6, even at low concentrations, and they then translocated into the nucleus (Figs. 4B ...
View Notes - Stat841f09 - Wiki Course Notes from STAT 441/8 stat 441/8 at University of Waterloo, Waterloo. 10/09/2013 Stat841 - Wiki Cour se Notes Stat841 From Wiki Cours e Notes Contents 1
кДНК STAT3 была впервые клонирована в 1994 году под именем APRF (англ. acute-phase response factor)[2]. В 1996 году была открыта укороченная изоформа мРНК STAT3, которая образуется в результате альтернативного сплайсинга. В этой мРНК отсутствует фрагмент длиной около 50 нуклеотидов, соответствующая изоформа белка называется STAT3β и является негативным регулятором транскрипции[3].. Полноразмерный белок STAT3α состоит из 770 аминокислотных остатков и имеет молекулярную массу около 92 кДа. Изоформа STAT3β имеет молекулярную массу около 80 кДа[4].. STAT3 имеет типичную для всех STAT-белков ...
Despite evidence implicating transcription factors, including STAT3, in oncogenesis, these proteins have been regarded as "undruggable." We developed a decoy targeting STAT3 and conducted a phase 0 trial. Expression levels of STAT3 target genes were decreased in head and neck cancers following injection with the STAT3 decoy compared with tumors receiving saline control. Decoys have not been amenable to systemic administration due to instability. To overcome this barrier, we linked the oligonucleotide strands using hexaethylene glycol spacers. This cyclic STAT3 decoy bound with high affinity to STAT3 protein, reduced cellular viability, and suppressed STAT3 target gene expression in cancer cells. Intravenous injection of the cyclic STAT3 decoy inhibited xenograft growth and downregulated STAT3 target genes in the tumors. These results provide the first demonstration of a successful strategy to inhibit tumor STAT3 signaling via systemic administration of a selective STAT3 inhibitor, thereby paving ...
STAT6 is a member of the STAT family of transcription factors. In response to cytokines and growth factors, STAT family members are phosphorylated by…
siRNA mediated knockdown of STAT3. A. Histogram of STAT3 levels in SW480 colon carcinoma cells treated with STAT3 and NTC (non-targeting) siRNAs. Red bars denot
Pub. L. 92-573, 86 Stat. 1207 (15 U.S.C. 2051-81) as amended by Pub. L. 94-284, 90 Stat. 503, Pub. L. 95-319, 92 Stat. 386, Pub. L. 95-631, 92 Stat. 3742; Pub. L. 90-189, 81 Stat. 568 (15 U.S.C. 1191-1204); Pub. L. 86-613, 74 Stat. 372, as amended by Pub. L. 89-756, 80 Stat. 1303, and Pub. L. 91-113, 83 Stat. 187 (15 U.S.C. 1261-74); Pub. L. 91-601, 84 Stat. 1670 (15 U.S.C. 1471-76) and the Act of Aug. 7, 1956, 70 Stat. 953 (15 U.S.C. 1211-14 ...
Finland Economic aid Stats", NationMaster. Retrieved from http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid. "Finland Economic aid Stats, NationMaster." 2008. ,http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid,.. Finland Economic aid Stats, NationMaster, ,http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid, [assessed 2008]. "Finland Economic aid Stats", NationMaster [Internet]. 2008. Avaliable from: ,http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid,.. "Finland Economic aid Stats", NationMaster. Avaliable at: nationmaster.com. Assessed 2008.. "Finland Economic aid Stats, NationMaster," http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid (assessed 2008). "Finland Economic aid Stats", NationMaster, http://www.nationmaster.com/country-info/profiles/Finland/Economy/Economic-aid (last visited 2008). "Finland Economic aid Stats", NationMaster, ...
Complete information for STAT2 gene (Protein Coding), Signal Transducer And Activator Of Transcription 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
... , Authors: Amanda M Del Rosario, Teresa M Bernaciak, Corinne M Silva. Published in: Atlas Genet Cytogenet Oncol Haematol.
The Ac2-26-mediated STAT3 activation is JAK-dependent and induces nuclear translocation and DNA binding of phosphorylated STAT3 as well as increased SOCS3 expre
View mouse Stat6 Chr10:127642986-127660957 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
View Notes - S479 F10 Test 2 Solutions from STAT 479 at Purdue. STAT 479 Test 2 November 9, 2010 1. You are given the following grouped claim information: Amount of Claim Number of Claims Total
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library(ggpubr) p ,- ggboxplot(ToothGrowth, x = supp, y = len, color = supp, palette = jco, add = jitter) p + stat_compare_means( aes(label = format.pval(..p.adj.., digits = 3)), label.x = 1.5, label.y = 40) ...
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x.shape = [1000, 2] # x[:, 0] ~ Uniform(0, 1), x[:, 1] ~ Uniform(1, 2). x = tf.stack([tf.random_uniform([1000]), 1 + tf.random_uniform([1000])], axis=-1) # edges ==, bins [0, 0.5), [0.5, 1.0), [1.0, 1.5), [1.5, 2.0]. edges = [0., 0.5, 1.0, 1.5, 2.0] tfp.stats.histogram(x, edges) ==, approximately [500, 500, 500, 500] tfp.stats.histogram(x, edges, axis=0) ==, approximately [[500, 500, 0, 0], [0, 0, 500, 500 ...
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Although the cytokine-inducible transcription factors STAT5a/b promote proliferation of a wide range of cell types, there are cell- and context specific cases in which loss of STAT5a/b results in enhanced cell proliferation. Here we report that loss of STAT5a/b from mouse embryonic fibroblasts (MEFs) leads to enhanced proliferation, which was linked to reduced levels of the cell cycle inhibitor p15INK4B and p21CIP1. We further demonstrate that growth hormone through the transcription factor STAT5a/b enhances expression of the cdkn2B gene and that STAT5a binds to GAS sites within the promoter. We have recently demonstrated that ablation of STAT5a/b from liver results in hepatocellular carcinoma upon a CCl4 insult. We also established that in liver tissue, like in MEFs, STAT5a/b activates expression of the cdkn2B gene. Loss of STAT5a/b led to diminished p15INK4B and increased hepatocyte proliferation. This study for the first time demonstrates that cytokines through STAT5a/b can induce the expression of a
Signal transducer and activator of transcription 3 (STAT3) is a transcription factor which in humans is encoded by the STAT3 gene. It is a member of the STAT protein family. STAT3 is a member of the STAT protein family. In response to cytokines and growth factors, STAT3 is phosphorylated by receptor-associated Janus kinases (JAK), form homo- or heterodimers, and translocate to the cell nucleus where they act as transcription activators. Specifically, STAT3 becomes activated after phosphorylation of tyrosine 705 in response to such ligands as interferons, epidermal growth factor (EGF), Interleukin (IL-)5 and IL-6. Additionally, activation of STAT3 may occur via phosphorylation of serine 727 by Mitogen-activated protein kinases (MAPK) and through c-src non-receptor tyrosine kinase. STAT3 mediates the expression of a variety of genes in response to cell stimuli, and thus plays a key role in many cellular processes such as cell growth and apoptosis. STAT3-deficient mouse embryos cannot develop ...
STAT1 mediates response to interferons and regulates immunity, cell proliferation, apoptosis, and sensitivity of Fanconi Anemia cells to apoptosis after interferon signaling; the roles of STAT1 in embryos, however, are not understood. To explore embryonic functions of STAT1, we investigated stat1b, an unstudied zebrafish co-ortholog of human STAT1. Zebrafish stat1a encodes all five domains of the human STAT1-alpha splice form but, like the human STAT1-beta splice variant, stat1b lacks a complete transactivation domain; thus, two unlinked zebrafish paralogs encode protein forms translated from two splice variants of a single human gene, as expected by sub functionalization after genome duplication. Phylogenetic and conserved synteny studies showed that stat1b and stat1a arose as duplicates in the teleost genome duplication (TGD) and clarified the evolutionary origin of STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B and STAT6 by tandem and genome duplication. RT-PCR revealed maternal expression of ...
Summary. To investigate the functions of signal transducers and activators of transcription 1 (STAT1)-induced anti-hepatitis C viral (HCV) effects, a stable Huh7.5 cell line (Huh7.5-STAT1ER) was established that constitutively expresses a fusion protein (STAT1ER) of STAT1 and the mouse oestrogen receptor (ER), which forms STAT1ER homodimers after 4-hydroxytamoxifen (4-HT) treatment. This inducible and cytokine/receptor-independent STAT1 activation system allowed us to investigate the anti-HCV effects of STAT1ER activation after inducing IFN-stimulated gene (ISG) expression. The anti-HCV effects of dimerized STAT1ER fusion protein were determined by real-time PCR in a time-dependent fashion post-HCV (JFH-1) infection. HCV (JFH-1) RNA decreased 48% at 72 h after 4-HT treatment. To distinguish the inhibitory effects of STAT1ER activation on HCV RNA replication or HCV internal ribosomal entry site (IRES)-mediated translation, a dicistronic pRL-HL construct was used in the studies. Both cellular ...
article{2983518, abstract = {Tyrosine phosphorylation is a hallmark for activation of STAT proteins, but their transcriptional activity also depends on other secondary modifications. Type I IFNs can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cell-specific, selective triggering of only the ISGF3 transcriptional program. Following a genome-wide RNAi screen, we identified the SIN3 transcription regulator homolog A (Sin3a) as an important mediator of this STAT3-targeted transcriptional repression. Sin3a directly interacts with STAT3 and promotes its deacetylation. SIN3A silencing results in a prolonged nuclear retention of activated STAT3 and enhances its recruitment to the SOCS3 promoter, concomitant with histone hyperacetylation and enhanced STAT3-dependent transcription. Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient IFN-mediated antiviral protection against influenza A and hepatitis C viruses. The Sin3a complex therefore acts ...
Interferon alpha (IFN-α) binds to a cell surface receptor that activates the Jak-Stat signaling pathway. A critical component of this pathway is the translocation of interferon stimulated gene factor 3 (a complex of three proteins Stat1, Stat2 and IRF9) to the nucleus to activate antiviral genes. A stable sub-genomic replicon cell line resistant to IFN-α was developed in which the nuclear translocation of Stat1 and Stat2 proteins was prevented due to the lack of phosphorylation; whereas the nuclear translocation of IRF9 protein was not affected. In this study, we sought to overcome defective Jak-Stat signaling and to induce an antiviral state in the IFN-α resistant replicon cell line by developing a chimera IRF9 protein fused with the trans activating domain (TAD) of either a Stat1 (IRF9-S1C) or Stat2 (IRF9-S2C) protein. We show here that intracellular expression of fusion proteins using the plasmid constructs of either IRF9-S1C or IRF9-S2C, in the IFN-α resistant cells, resulted in an increase in
The previous studies have shown that HCMV infection initiates a novel signal transduction pathway that leads to the induction of ISGs (35, 36). Later, it was discovered that the HCMV envelope glycoproteins, gB and gH, and subsequent virion fusion are required for this virus-induced activation (3, 19, 25). In this study, we demonstrated that ISRE and GAS elements are HCMV response sites (VRS). A number of cellular proteins are activated after HCMV infection that specifically interact with the VRS. These proteins have molecular masses between 19 and 41.7 kDa.. It was interesting and unexpected to determine that both ISRE and GAS elements, in fact, form identical complexes with HCMV-activated proteins. The ISRE normally interacts with IFN-α or -β-activated complexes or ISGF-3 containing Stat1, Stat2, and IRF-9 (p48). GAS normally interacts with the IFN-γ-activated Stat1 homodimer (6, 7). The fact that HCMV-activated complexes recognize both ISRE and GAS elements suggests that either a single ...